scholarly journals PCN147 MEDICAL RESOURCES UTILIZATION OF FIVE MOST PREVALENT CANCERS IN TAIWAN (LUNG CANCER, LIVER CANCER, COLORECTAL CANCER, GASTRIC CANCER, AND BREST CANCER): 2001~2007

2010 ◽  
Vol 13 (7) ◽  
pp. A279
Author(s):  
JS Liu ◽  
LT Chen ◽  
CF Hsiao
Author(s):  
Yating Xu ◽  
Xiao Yu ◽  
Menggang Zhang ◽  
Qingyuan Zheng ◽  
Zongzong Sun ◽  
...  

Long non-coding RNAs (lncRNAs) are RNAs with a length of no less than 200 nucleotides that are not translated into proteins. Accumulating evidence indicates that lncRNAs are pivotal regulators of biological processes in several diseases, particularly in several malignant tumors. Long intergenic non-protein coding RNA 1116 (LINC01116) is a lncRNA, whose aberrant expression is correlated with a variety of cancers, including lung cancer, gastric cancer, colorectal cancer, glioma, and osteosarcoma. LINC01116 plays a crucial role in facilitating cell proliferation, invasion, migration, and apoptosis. In addition, numerous studies have recently suggested that LINC01116 has emerged as a novel biomarker for prognosis and therapy in malignant tumors. Consequently, we summarize the clinical significance of LINC01116 associated with biological processes in various tumors and provide a hopeful orientation to guide clinical treatment of various cancers in future studies.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e13590-e13590
Author(s):  
Zhuang Yu ◽  
Jing Wang ◽  
Lingxin Feng ◽  
Xue Yang ◽  
Qi Qi ◽  
...  

e13590 Background: Immunotherapy is becoming one of the promising treatments for cancer administration, and several studies indicated a better outcome was received in patients with high tumor mutation burden (TMB). The distribution of TMB is still unknown and this study aimed to analysis the association between TMB and age especially in East Asian populations. Methods: In our study, TMB value was measured as the numbers of synonymous, nonsynonymous mutations and InDels by next generation sequencing with 539 genes panel in tumor tissue. TMB-H was defined as highest mutation load quintile (top 20%) in each cancer type. The association between TMB and age in 874 patients was investigated including 174 patients with liver cancer, 32 patients with bile duct cancer, 54 patients with gastric cancer, 119 patients with colorectal cancer, 27 patients with pancreatic cancer, 32 patients with melanoma, 25 patients with glioma and 411 patients with lung cancer cases, respectively. Spearman rank correlation analysis, Mann-Whitney U-test and Fisher’s exact test were used for statistical analysis. Results: A significant correlation between TMB and ages was observed in patients with solid tumors (r = 0.204, p = 1.263×10−9). The median age of included patients was 60 years-old. Based on nonparametric test, the value of TMB in patients with liver cancer ( p = 2.310×10−4), gastric cancer ( p = 0.029) and lung cancer ( p = 0.001) aged ≥ 60 years-old was significantly higher than the corresponding patients aged < 60 years-old. No significant differences of TMB values were found between patients < 60 and ≥ 60 years-old in bile duct cancer ( p = 0.419), colorectal cancer ( p = 0.075), pancreatic cancer ( p = 1), melanoma ( p = 0.952) and glioma ( p = 0.720). The TMB-H ratio in patients with liver ( p = 0.049) and gastric ( p = 0.015) cancer aged < 60 years old was significantly lower than patients aged ≥ 60 years-old. Conclusions: Our study indicated the TMB value and TMB-H ratio were relatively higher with ages ≥ 60 years old in specific tumors, which might provide useful information to guide precisely the the application of PD-1 or PD-L1 inhibitors. As a retrospective study with a relatively small population, the conclusions of this study needed to be verified with a larger sample.


2019 ◽  
Vol 18 (5) ◽  
pp. 18-28
Author(s):  
G. G. Khakimova ◽  
Zh. R. Cherkasova ◽  
S. A. Tsurkan ◽  
G. A. Fedchikov ◽  
N. V. Suganov ◽  
...  

The objective of the study was to assess the feasibility of using CA -62 marker of epithelial carcinomas for monitoring treatment response and detecting cancer progression or recurrence during chemotherapy.Material and Methods. A 12-month double-blind clinical trial was conducted by two independent groups: clinical oncologists and biochemists, and involved 89 patients with different cancers confirmed by histopathological findings. The other inclusion criteria were: the presence of at least one measurable lesion according to the RECIST criteria, ECOG performance status 0-2 and satisfactory laboratory parameters. The expression of CA -62 cancer marker was measured by immunochemiluminescent assay used for the detection of epithelial carcinomas.Results. The elevated level of CA -62 marker was observed in 76 patients before starting the treatment. After completion chemotherapy, the level of this marker decreased to the normal reference ranges (<4600 U/ml) in 53 % of patients and remained increased in 24 % of patients. Of 24 % of patients with the initial low level of CA -62 marker (1000–4000 U/ml) before treatment, 12 % had no changes in the level of this marker during chemotherapy; however, 5 % of these patients had disease progression and 7 % had stable disease after starting the treatment. In 12 % of patients with an initial low CA -62 level, it increased during chemotherapy, indicating disease progression.Conclusion. The changes in the level of CA -62 marker during chemotherapy in patients with gastric cancer, small-cell lung cancer, colorectal cancer, neuroendocrine cancer and ovarian cancer showed a high correlation (76–100 % depending on the tumor site) with the performance status of the patients according to RECIST criteria. The CA -62 marker was shown to be feasible for monitoring gastric cancer, small-cell lung cancer, colorectal cancer, neuroendocrine cancer and ovarian cancer as well as for assessing the response to chemotherapy.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15174-e15174
Author(s):  
Zhen Zhang ◽  
Xing Zhang ◽  
Minhui Ge ◽  
Huijuan Qin

e15174 Background: Microsatellite instability-high (MSI-H) is the gain or loss of nucleotides from repetitive DNA caused by genomic hypermutability and a powerfully predictive phenotype for diagnosis, immunotherapy and prognosis in various types of cancer. Herein, we analyze the frequency of MSI-H for the understanding of epidemiology of MSI-H across major types of human cancer. Methods: MSI value was calculated by bioinformatics algorithm based on NGS from 539 genes panel in tumor tissue. Patients were divided into three classes as MSI-H, MSI-L and MSS based on MSI value. MSI-H was defined as above 10% positive of the 195 tested microsatellites sites, and this method was totally consistent with conventional MSI-PCR testing in research and development sample verification. We compared the differences of MSI-H ratio in eight types of human cancer including liver cancer, bile duct cancer, gastric cancer, colorectal cancer, pancreatic cancer, melanoma, glioma and lung cancer from 874 cancer cases via χ2 test, adjusted standardized residual or Fisher's exact test. Results: The ratios of MSI-H in eight types of solid tumors were 0% in 32 patients with bile duct cancer or 27 patients with pancreatic cancer, 0.6% (1/174) in liver cancer, 1.9% (1/54) in gastric cancer, 6.7% (8/119) in colorectal cancer, 3.1% (1/32) in melanoma, 4% (1/25) in glioma, and 0.5% (2/411) in lung cancer, respectively. Significant correlations between the MSI-H and cancer types were found by χ2 test (χ2 = 26.571, Cramer’s V coefficient = 0.174, p = 3.980×10−4). Only patients with colorectal cancer had absolute values of adjusted standardized residual above 3, its observed counts of MSI-H significantly higher than expected counts. Fisher’s exact test was performed to analyze the differences of MSI-H ratio across hepatobiliary (liver and bile duct) cancer, digestive tract (gastric and colorectal) cancer and lung cancer, and we found the MSI-H ratio of patients with digestive duct cancer was significantly higher than patients with hepatobiliary cancer ( p = 0.007) or lung cancer ( p = 4.599×10−4). Conclusions: Our study provided new references to cancer-specific properties and clinical diagnosis of MSI especially in East Asian populations. As a retrospective study with a relatively small population, the conclusions of this study needed to be verified with a larger sample.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15170-e15170
Author(s):  
Peng Chen ◽  
Cuicui Zhang ◽  
Zhaoting Meng ◽  
Xing Zhang ◽  
Minhui Ge ◽  
...  

e15170 Background: Tumor mutational burden (TMB) is an impressive predictive biomarker for immune checkpoint inhibitors therapy, and immunotherapy is one of the most promising methods for cancer treatment. However, the profile of TMB in various types of cancers was still poorly understood. Methods: In this study, genomic profiling of DNA was performed using next generation sequencing from a 539 genes panel in tumor tissues. The TMB was defined as the numbers of SNVs including synonymous and nonsynonymous mutations, and InDels per megabase in coding regions of sequenced genome. TMB-H was defined as highest mutation load quintile (top 20%) in each cancer type. The values of TMB of 874 patients were compared among eight main tumor types including 174 patients with liver cancer, 32 patients with bile duct cancer, 54 patients with gastric cancer, 119 patients with colorectal cancer, 27 patients with pancreatic cancer, 32 patients with melanoma, 25 patients with glioma and 411 patients with lung cancer cases by multiple independent samples nonparametric Kruskal-Wallis H test via SPSS v22.0. Results: The median values of TMB in liver cancer, bile duct cancer, gastric cancer, colorectal cancer, pancreatic cancer, melanoma, glioma and lung cancer were 10.29, 8.09, 11.03, 10.29, 5.88, 7.35, 5.88 and 7.35 Muts/Mb, respectively. The cut-off values of TMB-H in corresponding eight solid tumors were 16.18, 19.12, 19.85, 16.18, 10.29, 13.24, 10.29 and 18.38 Muts/Mb, respectively. Based on nonparametric Kruskal-Wallis H test, there were significant differences of median TMB values across eight independent tumor types (χ2 = 26.752, p = 3.693×10−4). Significant differences between patients with colorectal cancer and pancreatic cancer ( p = 0.005) or lung cancer ( p = 0.011) were observed via pairwise comparisons. Conclusions: Our study proved the presence of significant differences across eight cancer types, deepened the knowledge of the cancer-specific of TMB, provided useful information in immunology therapy for East Asian patients with solid tumors. As a retrospective study with a relatively small population, the conclusions of this study needed to be verified with a larger sample.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15169-e15169
Author(s):  
ZHENG ZHAO ◽  
Wentao Li ◽  
Xing Zhang ◽  
Minhui Ge ◽  
Chao Song

e15169 Background: Both oftumor mutational burden (TMB) and microsatellite instability (MSI) are promising predictive biomarkers for immunotherapy in cancer treatment. However, the association between TMB and MSI with solid tumors was not well investigated especially in East Asian patients. Herein, the relationships for characterizing TMB and MSI in major cancer types were made. Methods: TMB and MSI were measured by 539 genes panel via NGS in tumor tissues. The TMB were calculated as the numbers of synonymous and nonsynonymous mutations, and InDels per megabase in coding regions. MSI was the gain or loss of nucleotides from repetitive DNA and the criteria of MSI-H were defined as above 10% positive of the 195 tested microsatellites sites, and this method was totally consistent with conventional MSI-PCR testing in Research and development sample verification. The relationships between TMB and MSI of 874 patients with solid tumors including 174 patients with liver cancer, 32 patients with bile duct cancer, 54 patients with gastric cancer, 119 patients with colorectal cancer, 27 patients with pancreatic cancer, 32 patients with melanoma, 25 patients with glioma and 411 patients with lung cancer cases were performed by Spearman rank correlation analysis via SPSS v22.0. Results: There was no significant correlation between TMB and MSI in total patients with solid tumors (r = 0.061, p = 0.073). Significantly correlations were observed in patients with colorectal cancer (r = 0.248, p = 0.006) and pancreatic cancer (r = 0.397, p = 0.040). Meanwhile, no significant correlations between TMB and MSI were identified in patients with liver cancer (r = -0.016, p = 0.830), bile duct cancer (r = 0.325, p = 0.070), gastric cancer (r = 0.209, p = 0.130), melanoma (r = -0.057, p = 0.757), glioma (r = 0.009, p = 0.967) and lung cancer (r = 0.015, p = 0.758). Interestingly, total eleven cases were confirmed as MSI high in patients with colorectal cancer, glioma and lung cancer all presented phenotypes of TMB high. Conclusions: We demonstrated the presence of tumor-specific properties correlations between TMB and MSI and provided new insights to use them as biomarkers in immunotherapy. As a retrospective study with a relatively small population, the conclusions of this study needed to be verified with a larger sample.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15176-e15176
Author(s):  
Shun Xu ◽  
Minqi Tian ◽  
Xing Zhang ◽  
Chuang Qi ◽  
Chao Song

e15176 Background: Programmed death-ligand (PD-L1) expression is an efficacy predictive biomarker in cancer immunotherapy. PD-1/PD-L1 axis can restore the host immunity against malignancies causing durable tumor remissions, and thus the level of PD-L1 protein expression is of critical clinical significance. However, the knowledge of PD-L1 expression level of patients with different malignancies is still inadequate understanding. Methods: Based on the percentage of positive tumor cells (TC value) identified by immunohistochemistry (IHC) method, the protein expression of PD-L1 was divided into three groups as g1 (TC < 1%), g2 (1% ≤ TC < 50%) and g3 (TC ≥ 50%). The expressions of PD-L1 from 1772 patients with malignancies across eight types including 133 patients with liver cancer, 35 patients with bile duct cancer, 94 patients with gastric cancer, 146 patients with colorectal cancer, 48 patients with pancreatic cancer, 76 patients with melanoma cancer, 33 patients with glioma and 1207 patients with lung cancer cases were made. The relationships between cancer types and PD-L1 expression were calculated via χ2 test using SPSS v22.0. Results: The ratios of PD-L1 expression in three groups (g1, g2 and g3, respectively) across eight cancer types were 67.7, 30.8 and 1.5% in liver cancer, 65.7, 28.6 and 5.7% in bile duct cancer, 77.7, 20.2 and 2.1% in gastric cancer, 81.5, 18.5 and 0% in colorectal cancer, 64.6, 31.2 and 4.2% in pancreatic cancer, 50.5, 35.7 and 13.8% in melanoma, 30.3, 63.1 and 6.6% in glioma and 55.9, 34.0, 10.1% in lung cancer, respectively. Significant correlation between the PD-L1 expression and cancer types were found (χ2 = 140.543, Cramer’s V coefficient = 0.199, p = 5.53×10−23). The expression of PD-L1 in patients with lung cancer tended to be distributed in g3, in patients with melanoma tended to be distributed in g2, and in patients with gastric cancer, glioma, and colorectal cancer tended to be distributed in g1. Conclusions: Our study suggested the protein expression of PD-L1 was significantly heterogeneous among various cancer types and offered new references for cancer-specific characters of PD-L1 expression. As a retrospective study with a relatively small population, the conclusions of this study needed to be verified with a larger sample.


2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Nan Zhang ◽  
Yuxin Zuo ◽  
Yu Peng ◽  
Lielian Zuo

N6-Methyladenosine (m6A) modification is a dynamic and reversible methylation modification at the N6-position of adenosine. As one of the most prevalent posttranscriptional methylation modifications of RNA, m6A modification participates in several mRNA processes, including nuclear export, splicing, translation, and degradation. Some proteins, such as METTL3, METTL14, WTAP, ALKBH5, FTO, and YTHDF1/2/3, are involved in methylation. These proteins are subdivided into writers (METTL3, METTL14, WTAP), erasers (ALKBH5, FTO), and readers (YTHDF1/2/3) according to their functions in m6A modification. Several studies have shown that abnormal m6A modification occurs in tumors, including colorectal cancer, liver cancer, breast cancer, nasopharyngeal carcinoma, and gastric cancer. The proteins for m6A modification are involved in tumor proliferation, angiogenesis, metastasis, immunity, and other processes. Herein, the roles of m6A modification in cancer are discussed, which will improve the understanding of tumorigenesis, as well as the diagnosis, treatment, and prognosis of tumors.


2021 ◽  
Vol 27 ◽  
Author(s):  
Qi Zhang ◽  
Yinxin Wu ◽  
Jinlan Chen ◽  
Yuxuan Cai ◽  
Bei Wang ◽  
...  

Background: MBNL1, a protein encoded by q25 gene on chromosome 3, belongs to the tissue-specific RNA metabolic regulation family, which controls RNA splicing.[1]MBNL1 formed in the process of development drive large transcriptomic changes in cell differentiation,[2] it serves as a kind of tumor differentiation inhibitory factor.MBNL1 has a close relationship with cancer, comprehensive analysis, [3]found that breast cancer, leukemia, stomach cancer, esophageal adenocarcinoma, glial cell carcinoma and another common tumor in the cut, and cut in Huntington's disease. But MBNL1 plays a promoting role in cervical cancer, is contradictory in colorectal cancer, It promotes colorectal cancer cell proliferation, On the other hand, it inhibits its metastasis, so it is an important physiological marker in many cancers. When we integrated the role of MBNL1 protein in various tumors, we found that its antisense RNA, MBNL1-AS1, had a good inhibitory effect in several colorectal cancer, non-small cell lung cancer, and gastric cancer. Objective: To elucidate the expression of MBNL1 and MBNL1-AS1 in various tumors, and to search for their physiological markers. Methods: It was searched by the PUMUB system and summarized its expression in various cancers. Results: MBNL1 was down-regulated, leukemia, breast cancer, glioblastoma, gastric cancer, overall survival rate, recurrence, metastasis increased. While the metastasis of colon cancer decreased, proliferation was promoted, and the effect of both was promoted for cervical cancer.MBNL1-AS1 was down-regulated, and the overall survival rate, recurrence, and metastasis of lung cancer, colorectal cancer, and bladder cancer increased. Conclusion: MBNL1 may be an important regulator of cancer, and MBNL1-AS1 is a better tumor suppressor.


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